How the Wrong Dietary Fat Can Wreck Your Health

STORY AT-A-GLANCE

• Omega-6 linoleic acid (LA) is the most common fat in the American diet. Most people get 25 times more LA than they need. At most, you need about 2 grams a day, but the average American gets about 50 grams a day, thanks to the fact that most processed foods and condiments are loaded with omega-6 seed oils

• LA gets incorporated into your cell membranes where it causes inflammation. Its half-life is nearly two years, so ridding your body of stored LA completely can take up to seven years

• Eliminating LA is a marathon, not a sprint. Ineffective and potentially harmful ways of eliminating LA include extended fasting and overtaxing your body with strenuous endurance exercise

• To stop the accumulation of LA in your cells, eliminate seed oils from your diet. Cook with beef tallow, butter, ghee or coconut oil, and avoid all processed foods, restaurant foods, condiments, and animals raised on grains, such as chicken and pork

• Vitamin E, in a dose of about 2 IU - 3 IU for every gram of PUFA (not just linoleate) consumed daily may also be able to provide some protection against the inflammatory and endocrine (estrogenic, pro-cortisol) effects of linoleate and PUFA in general

• To safely encourage the elimination of LA from your body, focus on building muscle and maximizing lean muscle mass with concentric exercise, and eat a balanced diet with a ratio of 2-to-1 healthy carbs to protein

In this interview, Georgi Dinkov, an expert on linoleic acid (LA), details some of the health hazards of this exceedingly common fat in the modern diet, and how to safely rid your body of it.

Both Georgi and I are convinced excessive LA intake is one of the most important variables that can make or break your health, especially in the long term. It's a far greater contributor to chronic and degenerative disease and mortality than sugar, and it's the primary culprit that makes processed foods so harmful.

The historical (last 50 to 75 years) incidence curves of cancer, cardiovascular disease (CVD), diabetes and neurological disease in the general population overlap remarkably well the ever-increasing PUFA consumption rates in developed countries, suggesting PUFA is a major factor in those diseases.1,2

How Georgi Became a Biohacker

Despite having a degree in computer science, Georgi has made a name for himself as an expert biohacker. After graduating from college in 2002, he got a job as a programmer at the National Biomedical Research Foundation (NBRF).

There, he helped develop uniprot.org, a database of all known protein sequences — Protein Information Resource (PIR — pir.georgetown.edu) and UniProt (www.uniprot.org).

Surrounded by up to 60 of the brightest doctors and biochemists in the world, Georgi developed an interest in biochemistry, and started studying on the side so he could more effectively collaborate with his coworkers. He provides an amazing example of what one can learn without any formal training if they merely apply themselves.

Low-Carb Considerations

In the interview, we clear up some of the pervasive confusion surrounding low-carb diets, and why long-term chronic low-carb is not ideal. It's a great short-term intervention for most people, especially those with insulin resistance.

This is because lowering carbs can help reset your metabolism and recover your metabolic flexibility. However, in the long term you can run into trouble — especially if you're also doing a lot of endurance training. The main reasons for the issues caused by chronic low-carb diets (and/or stress, which mimics the effects of low-carb diets) are:

1. The elevated lipolysis in a low carb-state, which results in chronically elevated circulating levels of PUFA, with the resulting inflammatory and endocrine effects (e.g. PUFA is pro-cortisol, estrogenic and also synergizes with endogenous/exogenous estrogens, and promotes their effects even in low doses).

2. The downregulation of the resting metabolic rate (RMR) by lowered synthesis of T3 when eating a low-carb diet and/or fasting and/or strenuous exercise.

For more details on this, be sure to listen to the interview at normal speed. Believe me, this is an interview that nearly everyone should listen to a few times to capture the incredible clinical pearls that Georgi shared. I personally learned more during this discussion than I have from most interviews.

If you listen to the interview, you will learn that once your sugar stores are expended, you start tapping into your fat stores through a process called lipolysis. This liberated fat is then circulated around your body and supplied to the cells as fuel to compensate for the low glucose availability.

However, certain types of fat block the effects of insulin in your body, so a long-distance endurance athlete can actually end up with a blood profile similar to that of a person with Type 2 diabetes. In Georgi's case, as an endurance athlete, his blood sugar climbed higher the less sugar he ate. This competition/antagonism between glucose and fats (mostly PUFA) as fuel for the cells was first discovered in the 1970s and named the Randle Cycle.

Why does it occur? The process in your liver that controls blood sugar is gluconeogenesis. If you stop supplying carbs to your body, the organs that need them will activate glucose creation in your body by elevating the stress hormone cortisol, which ends up being very destructive to your tissues, including skeletal muscle, liver, brain and kidneys.

In Type 2 diabetes, a state with hyperglycemia, only about 10% of the circulating glucose is of dietary origin. The rest is due to chronically elevated gluconeogenesis — which suggests that cortisol is the driver of hyperglycemia in Type 2 diabetes — and elevating cortisol chronically by doing low-carb or exhaustive exercise is likely detrimental to insulin sensitivity.

People with elevated cortisol (Cushing phenotype) have the same central obesity and loss of muscle mass (sarcopenia) as the ones seen in diabetes 2. Conversely, blocking cortisol's effects with the drug RU486 has been demonstrated to lead to sustained fat loss WITHOUT dieting, and improved insulin sensitivity.3,4,5

Cortisol goes up during exercise, and if there's no glucose around, cortisol rises even higher. Shakes, problem sleeping, jitteriness and neurological abnormalities are some of the symptoms of high cortisol and low glycogen stores. In Georgi's case, his symptoms slowly vanished once he started eating a more balanced diet, with a macronutrient ratio of about one-third carbs, one-third fat and one-third protein.

Dietary Fats and Fatty Liver Disease

In his search for answers to the symptoms he experienced on a low-carb diet, he came across Dr. Peat's website,6 aka, Dr. T.A. Peterson, an American biologist who's been studying the role of energy in the cell, and the effects of LA. Georgi started reading Peat's work in 2009, and eventually started doing his own experiments.

As noted by Georgi, published research has long demonstrated that LA is far from a benign macronutrient. It's actually a highly proinflammatory mediator and has endocrine effects that mimic estrogen. Contrary to popular belief, LA is also a major culprit in nonalcoholic fatty liver disease (NAFLD), more so than fructose and other sugars.7,8

Georgi cites research9,10,11 showing people with alcoholic cirrhosis (liver disease) who ate their normal diet, which was high in omega-6 fats, experienced classic progression of cirrhosis resulting in liver failure. The group whose diet was altered to eliminate all forms of fat aside from coconut oil, a saturated fat, was able to reverse their cirrhosis, even in the presence of continued alcohol abuse. Additional animal experiments12 confirmed these results. As explained by Georgi:

PUFAs Are Stored, Not Digested

An important take-home here is that PUFAs such as LA are not digested. Instead they're stored.13 Most of the body fat in obese individuals is composed of PUFAs, not saturated fat. Saturated dietary fat is mostly burned (oxidized) and used up.

So, obese individuals are typically not eating very much saturated fat; rather, they're exponentially overdosing on LA. Animal studies in the early 20th century demonstrated conclusively that pigs fed saturated fats (mostly coconut oil) could not get fat but became lean and muscular, while the ones fed PUFA gained mostly fat.

This led to the adoption/promotion of PUFA as animal feed since the goal there is to maximize "caloric efficiency" — i.e., get the animals as heavy as possible with a little food as possible. In other words, the pro-obesity effects of PUFA and anti-obesity effects of saturated fats are well-known in the livestock industry and are not disputed.

Considering the similarity of our metabolism/structure/tissues/organs with those of pigs, it should not be at all surprising that we keep getting fatter while consuming ever-larger amounts of PUFA.

The half-life of PUFAs such as LA, which get embedded and integrated into your cell membranes, is about 680 days. This means that to rid your body of LA will take approximately seven years, provided you don't load more in. And you really do want to get rid of this fat, as it's highly inflammatory and prevents your mitochondria and cellular machinery from operating properly.

Research has shown that given enough PUFAs, your cells will go into apoptosis, they basically commit suicide. "It can actually work like a radiation or chemotherapy. It is a type of chemotherapy," Georgi says. The implications14,15 of this insight are quite profound and I look forward to exploring that with Georgi on his next interview.

PUFAs Coming Out of Storage Can Cause Trouble

A key way to eventually lower your body burden of LA is to keep your total LA intake below 2%, maybe even close to 1%. You need to stop putting more in. Exercise and fasting will help drive the LA out, but you need to be really careful if you have a lot of LA storage.

My Recommendations for TRE Have Changed

Georgi pointed out the dangers of an excessive time-restricted eating (TRE) window.18,19,20,21,22,23,24,25 An extreme example of TRE is the one meal a day (OMAD) protocol, where you're fasting 20 hours or more each day. Georgi believes this is too extreme for most people, as most have large stores of LA that need to be purged safely.

I have been personally practicing and advocating a six– to eight-hour time restricted eating window. What I learned from our conversation is that this, or even longer eating restrictions and fasts, are perfectly appropriate for 95% of the population as they are insulin resistant and metabolically inflexible.

The major problem comes once you lose your insulin resistance and become metabolically flexible. At that point, this strategy becomes counterproductive as you will increase your cortisol levels, which causes chronic inflammation that can lead to tissue damage. Usually, it takes about three to six months for you to recover your metabolic flexibility.

Prior to my interview with Georgi I would have a six- to eight-hour eating window and I did this for a few years. Now I am going to shift to one day a week of 12 hours, three days of 10 hours and three days of eight hours. If you are metabolically healthy, I would encourage you to avoid very short eating windows under eight hours.

This is because chronic fasting also elevates your cortisol, just like chronic endurance exercise does. Cortisol, in turn, is involved in insulin resistance and the synthesis of fat, and promotes the storage of fat. Also, as just mentioned above, high amounts of LA can kill your cells.

This is a massive piece of the puzzle that I never fully appreciated. Molecular biology and pH physiology are based on a pre-1860s scenario where you didn't have these high levels of LA, which totally distorts the strategies. If they weren't there, you could fast to activate autophagy and get all these benefits.

You could have a much longer TRE window. But LA is a game changer. It radically modifies the concept of what you need to do to optimize your health. Essentially, if you've filled up your fat stores with LA — and in most people, over 20% of their fats are LA stored in their cell membranes and the optimum is 1% to 2% — then you need to integrate that knowledge into your strategy.

How to Safely Purge LA

How can you safely reduce these stores of LA without self-sabotaging? As explained by Georgi, extensive fasting will, in this instance, backfire, as will overtaxing yourself with heavy exercise. You'll need to accept that this is a marathon, not a sprint, and that it's going to take years to purge your LA stores. The best strategy, Georgi says, is to build muscle and maximize lean muscle mass.

Also avoid all processed foods, restaurant foods, condiments and animal foods raised on grains, such as chicken and pork. Aside from switching the types of dietary fats you eat, Georgi recommends a diet with a 2-to-1 ratio of carbs to protein, the carbs being in the form of fruits and vegetables, not processed sugary snacks.

Hopefully you didn't skim this and miss the pearl at the end, to take twice as many carbs as protein. What Georgi didn't state here, though, is that is for people who are metabolically flexible and not insulin resistant.

So, the key is not to be afraid of healthy carbs: They are your friend. If you are eating enough protein to build muscle, please make sure you also have enough carbs because, if you fail to do this, you can hurt your kidneys, liver and brain.

He also shared another pearl about resistance exercises that I wasn't aware of. Eccentric exercise, in which you are resisting gravity on the way down, builds muscles, BUT it also damages your muscles and destroys the mitochondria. It is far better to focus on the concentric phase of exercise, as it builds more and stronger mitochondria. Concentric exercise increase mitochondrial biogenesis, and steroidogenesis in muscle.26

How PUFAs Cause Heart Disease

Saturated fats improve the structure of cells, specifically the lipid bilayer, while PUFAs like LA impair it. The reason your cholesterol and LDL levels may go up when switching to saturated fats is because you're giving the cells the structural material needed, from which the cells can synthesize their own cholesterol as needed. Hence, extra cholesterol gets dumped into the bloodstream because it isn't needed.

Cholesterol is carried around by LDL. So, when you're eating saturated fat, your LDL rises, but it's rising because the cholesterol already in the cell is not as needed anymore. It's actually a good sign.

Conversely, when you're eating PUFAs, your cells need more cholesterol to strengthen their structure, so your body dumps cholesterol into the cells to protect them from the onslaught of the PUFAs. Hence, it appears your cholesterol level is going down, but it's actually having a strongly negative effect.

Additionally, the LA becomes oxidized and the LDL carrying it is now oxidized LDL, which is strongly associated with plaque. Plaque, associated with heart attacks also contains white blood cells, calcium, 7-ketocholesterol and PUFA peroxidation byproducts. Saturated fat does not contribute to plaque.

Concluding Thoughts

Like me, Georgi is convinced LA is a primary culprit in chronic diseases. And, since LA is found in most whole foods, there's really never any need to take an omega-6 supplement. It's virtually impossible to get too little from your diet.

I believe omega-6 supplements really ought to be removed from the market altogether, as people are getting 25 times more omega-6 than they could possibly need from their diet. At most, you need about 2 grams a day, but the average American gets about 50 grams a day, thanks to the fact that most processed foods and condiments are loaded with omega-6 seed oils.

If our diet were to be shifted away from seed oils to saturated fats, the way it was 150 years ago, we'd likely see a massive decline in chronic diseases, including cancer and heart disease.

To learn more, be sure to listen to the entire interview, as we dive into far greater detail than what I’ve summarized here. Georgi is an absolute fire hydrant when it comes to biochemical details. Also check out Georgi’s blog at www.haidut.me. You can also obtain a major sampling of Ray Peat’s work for free by going to these two sites: wiki.chadnet.org/Ray-Peat and RayPeat.com.